ArticleJournal of toxicology2025
Effect of Catechin on Hepatotoxicity Induced by Combined Doxorubicin and Paclitaxel Treatment.
Article in Journal of toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Hepatoprotective effect of dipyridamole against cyclophosphamide-induced hepatotoxicity in rats.Open veterinary journal · 2026Article
- Myricetin protects against doxorubicin-induced liver damage by modulating oxidative and inflammatory pathways.BMC pharmacology & toxicology · 2026Article
- Renal protective effect of coenzyme Q10 against methotrexate-induced nephrotoxicity in rats.Open veterinary journal · 2026Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemotherapy-induced hepatotoxicity remains a significant challenge in cancer treatment, limiting the clinical use of potent anticancer agents like doxorubicin (DOX) and paclitaxel (PAC). This study investigated the hepatoprotective effects of catechin (CAT), a natural flavonoid antioxidant, against DOX- and PAC-induced liver toxicity. Male Wistar rats were divided into five groups: control, DOX + PAC-treated, CAT-only, and two groups receiving CAT (20 or 40 mg/kg) in combination with DOX + PAC. Hepatic function was assessed through liver enzyme levels, oxidative stress biomarkers, and histopathological examination. Results showed that DOX + PAC treatment significantly elevated serum levels of ALT, AST, and ALP, indicating hepatocellular damage. Oxidative stress markers, including malondialdehyde (MDA) and nuclear factor kappa B (NF-κB), were also increased, while antioxidant defenses such as glutathione (GSH) and catalase were depleted. CAT coadministration, particularly at 40 mg/kg, markedly reduced oxidative damage, restored hepatic enzyme levels, and mitigated histopathological alterations, including congestion, hepatocyte degeneration, and inflammatory infiltration. Moreover, CAT reduced NF-κB expression, suggesting an anti-inflammatory effect. These findings demonstrate that CAT effectively protects against DOX- and PAC-induced hepatotoxicity by enhancing antioxidant defense mechanisms and reducing inflammation. Given its hepatoprotective potential, CAT may serve as a complementary therapeutic strategy to enhance chemotherapy tolerance.
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Registered trials
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